3.5.4.25: GTP cyclohydrolase II
This is an abbreviated version!
For detailed information about GTP cyclohydrolase II, go to the full flat file.
Word Map on EC 3.5.4.25
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3.5.4.25
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riboflavin
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anti-hcv
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lumazine
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guilliermondii
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famata
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gtp-cyclohydrolase
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2,5-diamino-6-ribosylamino-43h-pyrimidinone
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flavinogenic
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6,7-dimethyl-8-ribityllumazine
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pharmacology
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synthesis
- 3.5.4.25
- riboflavin
-
anti-hcv
- lumazine
- guilliermondii
- famata
-
gtp-cyclohydrolase
-
2,5-diamino-6-ribosylamino-43h-pyrimidinone
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flavinogenic
- 6,7-dimethyl-8-ribityllumazine
- pharmacology
- synthesis
Reaction
Synonyms
3,4-dihydroxy-2-butanone 4-phosphate synthase, GCH II, GCH II/III, GCH-II, gch2, GCHII, GTP 7,8-8,9-dihydrolase (diphosphate-forming), GTP cyclohydrolase 2, GTP cyclohydrolase II, GTP cyclohydrolase-II, GTP-8-formylhydrolase, GTPCH II, GTPCH-II, guanosine triphosphate cyclohydrolase II, guanosine triphosphate cyclohydrolase II/3,4-dihydroxy-2-butanone-4-phosphate synthase, guanosine-5'-triphosphate cyclohydrolase-II, More, NbRibA, ribA, ribA2, RIBIV, ToxB
ECTree
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Engineering
Engineering on EC 3.5.4.25 - GTP cyclohydrolase II
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Y210C/A290T/Q293R/A296T/K322R/F339Y/M361I
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the mutant shows a 2fold increase in GTP cyclohydrolase II activity and a 4fold increase in the Km value with GTP as the substrate. Using 2-amino-5-formylamino-6-ribosylamino-4(3H)-pyrimidinone 5'-triphosphate as the substrate, the mutant shows a rate enhancement by a factor of about 2 and an increase in the Km value by a factor of about 5
Y210C/A290T/Q293R/A296T/K322R/M361I
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the mutant shows increased kcat and Km values compared to the wild type enzyme using GTP and 2-amino-5-formylamino-6-ribosylamino-4(3H)-pyrimidinone 5'-triphosphate as the substrate
C54S
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site-directed mutagenesis, mutation results in proteins devoid of bound zinc and unable to release formate from the imidazole ring of GTP or from the intermediate analogue 2-amino-5-formylamino-6-ribosylamino-4(3H)-pyrimidinone 5'-triphosphate, however, the mutant enzyme is still capable to release diphosphate from GTP and from the formamide-type intermediate analogue
C65S
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site-directed mutagenesis, mutation results in proteins devoid of bound zinc and unable to release formate from the imidazole ring of GTP or from the intermediate analogue 2-amino-5-formylamino-6-ribosylamino-4(3H)-pyrimidinone 5'-triphosphate, however, the mutant enzyme is still capable to release diphosphate from GTP and from the formamide-type intermediate analogue
C67S
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site-directed mutagenesis, mutation results in proteins devoid of bound zinc and unable to release formate from the imidazole ring of GTP or from the intermediate analogue 2-amino-5-formylamino-6-ribosylamino-4(3H)-pyrimidinone 5'-triphosphate, however, the mutant enzyme is still capable to release diphosphate from GTP and from the formamide-type intermediate analogue
D127A
about 10fold less efficient than the wild-type protein
G209D
about 10fold less efficient than the wild-type protein
R83H
mutant substantially impaired in overall activity
Y123M
about 10fold less efficient than the wild-type protein, produces exclusively 2-amino-5-formylamino-6-ribosylamino-4(3H)-pyrimidinone 5'-phosphate
Y326F
generated by site-directed mutagenesis, catalytically inactive variant
Y326M
generated by site-directed mutagenesis, catalytically inactive variant
additional information
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an additional single copy of the ribA gene introduced into the sacBlocus of the riboflavin production strain and constitutive expression from the medium strength vegI promoter leads to improved riboflavin titers and yields of riboflavin on glucose of up to 25%, strain VB2XL1, both enzymatic activities of RibA, the 3,4-dihydroxy-2-butanone 4-phosphate synthase activity located in the N-terminal half of the protein and the GTP cyclohydrolase II activity of the C-terminal domain, are necessary for the improved riboflavin productivity, method, overview
additional information
generation of NbRibA-silenced plants via inoculation with Agrobacterium tumefaciens containing inf1, NbMEK2DD or Bax, or GUS as a control. Silencing NbRibA does not affect the activation of SIPK and defense-related genes, except for NbGST, effects of silencing NbRibA on disease resistance, phenotype
additional information
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generation of NbRibA-silenced plants via inoculation with Agrobacterium tumefaciens containing inf1, NbMEK2DD or Bax, or GUS as a control. Silencing NbRibA does not affect the activation of SIPK and defense-related genes, except for NbGST, effects of silencing NbRibA on disease resistance, phenotype
additional information
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the M120T variant of GCH II/II SCO 6655 acquires the ability to catalyze the conversion of GTP to 2,5-diamino-6-ribosylamino-4(3H)-pyrimidinone 5'-phosphate